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肥胖激素与痴呆。

Adiposity hormones and dementia.

机构信息

Section for Psychiatry and Neurochemistry, Neuropsychiatric Epidemiology Unit at the Sahlgrenska Academy, University of Gothenburg, Sweden.

出版信息

J Neurol Sci. 2010 Dec 15;299(1-2):30-4. doi: 10.1016/j.jns.2010.08.036. Epub 2010 Sep 27.

DOI:10.1016/j.jns.2010.08.036
PMID:20875649
Abstract

Adipose tissue is an endocrine and paracrine organ that contributes to both metabolic and vascular homeostasis. Overweight and obesity due to excess adipose tissue, are cornerstones of vascular risk and increase risk for late-onset dementia. Vascular risk does not exist in isolation, and is accompanied by alterations in hormonal metabolism and metabolic syndromes. Thus, while vascular risk is highlighted as a primary mechanism for elevated dementia occurrence due to obesity, hormonal risk states may also precede or result from underlying dementia-related neuropathologies and direct neuronal toxicity. This is exemplified during the prodromal phase of dementia, as vascular and metabolic parameters decline in relation to dementia development, and potentially in a way that is different from 'normal' aging. In this review will be presented a review of the epidemiology of adiposity and dementia; adipose tissue biology; and two major hormones produced by adipose tissue, leptin and adiponectin, that interact directly with the brain. In addition, a synthesis related to other lines of supporting evidence for the role of adipose hormones in dementia will be provided. Understanding the role of adipose tissue in health of the brain is pivotal to a deeper understanding of dementia processes.

摘要

脂肪组织是一种内分泌和旁分泌器官,有助于代谢和血管内环境的稳定。超重和肥胖是由于脂肪组织过多引起的,是血管风险的基石,并增加了迟发性痴呆的风险。血管风险并不是孤立存在的,还伴随着激素代谢和代谢综合征的改变。因此,尽管肥胖导致痴呆的血管风险被强调为主要机制,但激素风险状态也可能先于或由潜在的与痴呆相关的神经病理学和直接神经元毒性引起。这在痴呆的前驱期得到了例证,因为血管和代谢参数与痴呆的发展相关下降,并且可能与“正常”衰老的方式不同。在这篇综述中,将对肥胖症和痴呆的流行病学、脂肪组织生物学以及脂肪组织产生的两种主要激素——瘦素和脂联素进行综述,这些激素直接与大脑相互作用。此外,还将提供与支持脂肪激素在痴呆中作用的其他相关证据的综合分析。了解脂肪组织在大脑健康中的作用对于深入了解痴呆过程至关重要。

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